Animal models of Parkinson’s disease: limits and relevance to neuroprotection studies.

Erwan Bezard, Zhenyu Yue, Deniz Kirik, Maria Grazia Spillantini
Mov Disord. 2012-07-02; 28(1): 61-70
DOI: 10.1002/mds.25108

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1. Mov Disord. 2013 Jan;28(1):61-70. doi: 10.1002/mds.25108. Epub 2012 Jul 2.

Animal models of Parkinson’s disease: limits and relevance to neuroprotection

Bezard E(1), Yue Z, Kirik D, Spillantini MG.

Author information:
(1)University de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293,
Bordeaux, France.

Over the last two decades, significant strides has been made toward acquiring a
better knowledge of both the etiology and pathogenesis of Parkinson’s disease
(PD). Experimental models are of paramount importance to obtain greater insights
into the pathogenesis of the disease. Thus far, neurotoxin-based animal models
have been the most popular tools employed to produce selective neuronal death in
both in vitro and in vivo systems. These models have been commonly referred to as
the pathogenic models. The current trend in modeling PD revolves around what can
be called the disease gene-based models or etiologic models. The value of
utilizing multiple models with a different mechanism of insult rests on the
premise that dopamine-producing neurons die by stereotyped cascades that can be
activated by a range of insults, from neurotoxins to downregulation and
overexpression of disease-related genes. In this position article, we present the
relevance of both pathogenic and etiologic models as well as the concept of
clinically relevant designs that, we argue, should be utilized in the preclinical
development phase of new neuroprotective therapies before embarking into clinical

Copyright © 2013 Movement Disorders Society.

DOI: 10.1002/mds.25108
PMCID: PMC3517687
PMID: 22753348 [Indexed for MEDLINE]

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